Human Herpes Viruses in Patients with Chronic Periodontitis and Aggressive Periodontitis

Abstract

The pathogenesis of periodontal disease is a multifactorial process characterized by a complex interaction between the microbial and host factors and a variety of diseasemodulatory environmental factors [1]. Recent microbiological researches on periodontal disease are focused on the possible involvement of human viruses in the etiology and pathogenesis of destructive periodontal diseases [2-5]. Herpes viruses are frequently found in periodontal pockets and may initiate or accelerate periodontal tissue destruction because of a virally mediated release of cytokines or even an impairment of the periodontal tissue defense mechanism, resulting in a heightened virulence of resident pathogenic bacteria [6-8]. Human herpes viruses are classified into eight distinct species: Herpes simplex virus (HSV) 1 and 2, Varicella zoster virus (VZV), Human Cytomegalovirus (HCMV), Epstein Barr Virus (EBV) and human Herpes virus 6, human Herpes virus 7, and human Herpes virus 8 or Karposi's sarcoma-associated herpes virus [9]. Human cytomegalovirus (HCMV) and Epstien barr virus 1 (EBV-1) are involved in the pathogenesis of human periodontal disease. These viruses are capable of infecting and impairing Poly Morpho Nuclear Leukocytes (PMNs), macrophages and lymphocytes. Human cytomegalovirus may contribute to disease progression through the activation of IL1β gene transcription [10]. The reduced host defense by herpes virus-infected cells give rise to overgrowth of pathogenic bacteria that invade the periodontal tissue more efficiently [2].